Contact Information:
Department of Pathology & Laboratory Medicine
University of Kansas Medical Center
3901 Rainbow Boulevard, MS 1053
1033 Lied
Kansas City, KS 66160
Phone: (913) 588-7236
Fax: (913) 588-8287
Email: spaul2@kumc.edu
Office: 1033 Lied
Labs: 1016, 1019 Lied
Ph.D., University of Calcutta, 2002
Postdoctoral, University of Wisconsin Madison, 2002-2007
Assistant Professor:
Department of Pathology & Laboratory Medicine
Institute of Maternal-Fetal Biology
Division of Cancer & Developmental Biology
Angiogenesis, the development of new blood vessels from existing vasculature, is a key event in many physiological processes, like organ growth and development, wound healing, and reproduction, and is also critical for certain pathological disorders including tumor growth/metastasis, rheumatoid arthritis, diabetic retinopathy, atherosclerosis, psoriasis etc. Establishment of the angiogenic response that initiates blood vessel development and remodeling requires an exquisite balance between the activities of endogenous pro- and anti-angiogenic factors, which regulate endothelial cell function. However, the logic that permits complex signal integration by vascular endothelium is poorly understood. Our long-term research interest is to unravel the regulation and function of key genes that mediate development, survival, proliferation, migration, and invasion of endothelial cells in response to pro-and anti-angiogenic factors.
A major area of focus in the laboratory is to understand the transcriptional regulation of VEGF receptor 1 (VEGFR1), and VEGF receptor 2 (VEGFR2) during vasculogenesis, and physiological / pathological angiogenesis. We have discovered that, in isolated endothelial cells, pro- and anti-angiogenic signals modulate transcription of both VEGFR1 and VEGFR2. We want to study how a transcriptionally active VEGFR1 and VEGFR2 chromatin domain is established, maintained, and repressed. The major strategy is to define the native nucleoprotein structure of entire chromosomal regions and to elucidate factors/signals that establish this structure. Our study will involve isolated endothelial cells, ES cell differentiation system, Xenograft tumor models, and will be extended by genetic approaches in knockout and transgenic models.
Pal, S., Wu, J., Murray, J. K., Gellman, S. H., Wozniak, M. A., Keely, P. J., Boyer, M. E., Gomez, T. M., Hasso, S. M., Fallon J. F., and Bresnick, E. H. (2006) An Anti-Angiogenic Neurokinin-B/Thromboxane A2 Regulatory Axis. J. Cell Biol. 174:1047-1058.
Grass, J. A., Jing, H., Kim, S. L., Martowicz, M. L., Pal, S., Blobel G. A., and Bresnick, E. H. (2006) Hematopoietic Regulation via GATA Factor Complexes Dispersed Over Broad Region of the GATA-2 Chromatin Domain. Mol. Cell Biol. 26:7056-7067.
Pal, S., Nemeth, M. J., Bodine, D., Miller, J. L., Svaren, J., Thein, S. L., Lowry, P. J., and Bresnick, E. H. (2004) Neurokinin-B transcription in erythroid cells: Direct activation by the hematopoietic transcription factor GATA-1. J. Biol. Chem. 279:31348-31356.
Pal, S, Cantor, A. B., Johnson, K. D., Moran, T. B., Boyer, M. E., Orkin, S. H. and Bresnick, E. H. (2004) Coregulator-dependent facilitation of chromatin occupancy by GATA-1. Proc. Natl. Acad. Sci. U.S.A. 101: 980-985.
Grass, J. A., Boyer, M. E., Pal, S., Wu, J., Weiss, M. J., and Bresnick, E. H. (2003) GATA-1-dependent transcriptional repression of GATA-2 via disruption of positive autoregulation and domain-wide chromatin remodeling. Proc. Natl. Acad. Sci. U.S.A. 100: 8811-8816.
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